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This chapter provides a review of the vast body of published research that has used either structural magnetic resonance imaging (MRI) or diffusion tensor imaging (DTI) to investigate for neuroanatomical abnormalities in schizophrenia (SZ) patients. If one thing is clear from the multitude of MRI and DTI studies reviewed in the chapter, it is that there is now a great deal of evidence indicating that SZ patients exhibit consistent (albeit subtle) and widespread abnormalities in both their gray matter (GM) and white matter (WM). An important question, then, is whether these GM and WM abnormalities have separate causes, or whether they share a common underlying pathology. A highly speculative theory is presented as to how a single mechanism could potentially underlie the GM abnormalities, WM abnormalities, hyperdopaminergia and psychotic features characteristic of SZ. This theory is extremely speculative and would benefit from a great deal more supporting empirical evidence.
This chapter reviews magnetic resonance imaging (MRI) findings on developmental disabilities that arise from both modular and distributed perspectives on brain function, although the former clearly represent the majority of existing data. It focuses exclusively on autism spectrum disorders (ASD) including the diagnoses of autism, Asperger's Syndrome, and pervasive developmental disorder. Some evidence indicates that observed abnormalities in language areas may reflect different processing styles, rather than deficits per se. Visual information processing has always been a topic of great interest to ASD researchers, as individuals with ASD often show preserved and sometimes enhanced visual abilities. A large number of studies have established the role of superior temporal sulcus in various aspects of social perception. Mirror neuron system (MNS) has proven responsive to both the perception and implementation of specific body movements. The relatively high spatial resolution of MRI lends itself very well to the isolation of specific brain structures.
The computational anatomy techniques enable us to detect and to visualize discrete changes in cortical and hippocampal integrity and to track the spread of Alzheimer's disease (AD) pathology throughout the living brain. This chapter focuses on the new generation of cortical and hippocampal mapping techniques, while reviewing the research findings reported in the literature. The computational anatomy field is based on mathematical approaches for modeling anatomical structures in brain images. 3D surface-based analyses have documented the relentless progression of AD pathology-driven changes from pre-dementia of the Alzheimer's type (DAT) to moderate DAT. An important utility of the cortical mapping approaches is the exploration of brain-behavior correlations. For decades, DAT clinical trial design has relied solely on cognitive and functional outcome measures. A major advantage of computational anatomy techniques is to track the disease process in 3D, revealing the dynamic sequence in which brain structures are affected.
Martha E. Shenton, VA Boston Healthcare System and Department of Psychiatry Brigham and Women's Hospital Harvard Medical School Boston, MA, USA,
Bruce I. Turetsky, Department of Psychiatry University of Pennsylvania School of Medicine Philadelphia, PA, USA
Historically, the opportunity to examine the inner workings of the human body was limited to the study of cadavers. In the past 30 years, medical imaging technology has provided researchers with a new window into the living human body. Advances in medical imaging technology have, in fact, truly revolutionized nearly every area of medicine. These advances include both dramatic improvements in image resolution and the development of novel imaging techniques, from computed axial tomography (CT), to positron emission tomography (PET), to single photon emission tomography (SPECT), to magnetic resonance imaging (MRI), including fMRI (functional MRI) and diffusion tensor imaging (DTI), to magnetic resonance spectroscopy (MRS), ultrasound, and magnetoencephalography (MEG) – all of which provide an unprecedented view, in exquisite detail, of anatomical structures and/or functions in the living human body.
One medical discipline that has been in the forefront of this revolution is neuropsychiatry (defined here as encompassing both psychiatry and behavioral neurology), where novel neuroimaging tools have been developed and applied to neuropsychiatric disorders in order to understand further the neuroanatomical and neurophysiological bases of mental illnesses and cognitive disorders, including Alzheimer's and Parkinson's diseases.
This book reviews important new findings about the role of brain abnormalities in neuropsychiatric disorders based on this new imaging technology. In considering the progress in this area, it is clear that initially the quest was to identify and characterize focal brain abnormalities in an effort to delineate further various psychiatric and neuropsychiatric syndromes.
An informative and comprehensive review from the leading researchers in the field, this book provides a complete one-stop guide to neuroimaging techniques and their application to a wide range of neuropsychiatric disorders. For each disorder or group of disorders, separate chapters review the most up-to-date findings from structural imaging, functional imaging and/or molecular imaging. Each section ends with an overview from a internationally-renowned luminary in the field, addressing the question of 'What do we know and where are we going?' Richly illustrated throughout, each chapter includes a 'summary box', providing readers with explicit take-home messages. This is an essential resource for clinicians, researchers and trainees who want to learn how neuroimaging tools lead to new discoveries about brain and behaviour associations in neuropsychiatric disorders.
The conceptual framework of the pathophysiology and etiology of the eating disorders (EDs) anorexia nervosa (AN), bulimia nervosa (BN) as well as the emerging ED binge eating disorder (BED), has undergone significant changes in the past few decades. Structural imaging techniques such as computer tomography (CT) and radiation-free magnetic resonance imaging (MRI) provide information on gross structural abnormalities. Quantitative electroencephalography (qEEG) studies have recently come to prominence as a functional assessment method. Functional brain imaging is performed in conjunction with paradigms and tasks that are meant to elicit areas of brain activation that might be specific for AN pathophysiology. Many different paradigms have been used over the past years, with positron emission tomography (PET) and single photon emission computed tomography (SPECT) comprising the earlier work and functional MRI achieving prominence more recently. A mixed group of AN and BN subjects had reduced prefrontal myo-inositol and lipid compounds compared to controls.
Alcoholism is frequently accompanied by comorbidities of drugs of abuse and psychiatric diseases. For example, individuals with schizophrenia are at increased risk for developing substance abuse disorders. The availability of imaging tools has enhanced the appreciation of the effects of chronic and excessive alcohol exposure on the human brain. In-vivo computerized tomography (CT) and magnetic resonance imaging (MRI) studies of alcoholism complement postmortem neuropathological investigations in the search for structural brain abnormalities due to alcoholism. This chapter first reviews the general principles of brain imaging and of images analyses as they pertain to the characterization of appropriate structural regions. Then, it reviews the literature on the effects of alcoholism on brain structure as revealed by brain imaging. In combination with structural imaging, experimental models of alcoholism could be a translational point in identifying mechanisms of alcohol-related brain dysmorphology.
Post-traumatic stress disorder (PTSD) includes a constellation of disabling behavioral and emotional symptoms that occur in a proportion of individuals exposed to severe psychological trauma. This chapter reviews the structural neuroimaging findings pertaining to specific brain regions in adults with PTSD. Although the majority of adult neuroimaging reports have centered on the hippocampus, medial prefrontal cortex, and amygdala, structural studies are potential abnormalities in other brain regions as well. The cavum septum pelucidum (CSP), a small cerebrospinal fluid filled cleft in the anterior portion of the septo-callosal junction, has been found to exist with greater frequency in individuals diagnosed with PTSD. Pediatric studies of PTSD have not fully replicated findings reported in the adult literature, and suggest that the neuroanatomical correlates of PTSD may manifest in a more generalized manner in children and adolescents who are traumatized.
This chapter discusses recent structural neuroimaging studies that address the regions of interest in the proposed anterior limbic network model. Given the predominance of MRI in structural imaging of psychiatric disorders, the chapter also focuses on this imaging modality. First, longitudinal studies are needed to clarify how brain structures change within individual patients, with particular regard to the corresponding course of illness. Second, more sophisticated measures, such as diffusion tensor imaging (DTI) tractography or shape analyses, may more consistently define the subtle structural abnormalities that are likely in bipolar disorder and that may be missed with less-specific measures. Third, studies in young patients are critical given the typical adolescent onset of bipolar disorder and early course progression. Finally, integrating structural imaging with functional and neurochemical are the only ways to move morphometric imaging from high-priced and sophisticated phrenology to a better understanding of the neural basis of bipolar disorder.
Norepinephrine is believed to modulate CNS processing of
environmental signals. However, its specific role in stimulus
evaluation processes has not been delineated. We examined the
effects of the α2 noradrenergic agents, clonidine
and yohimbine, on ERP and performance measures of auditory
information processing. Ten healthy participants performed a
three-tone target detection experiment, receiving either placebo,
0.2 mg clonidine, or 30 mg yohimbine, in a double-blind randomized
design. The principal locus of action of the noradrenergic agents
occurred between 100 and 200 ms poststimulus. P200 latency was
sped by yohimbine and slowed by clonidine, and the frontal P3a
was shifted in tandem. Components related to target detection
(N250 and P3b) were unaffected. The results suggest that
norepinephrine modulates CNS mechanisms of selective attention
to infrequent stimuli. This may be relevant for patients with
schizophrenia, a subset of whom exhibit selective abnormalities
of these same ERP components. Our results offer a possible link
between these two sets of findings, suggesting that some patients
with schizophrenia may have dysfunctional noradrenergic systems.
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